Long non-coding RNA MALAT1 interacts with transcription factor Foxo1 to regulate SIRT1 transcription in high glucose-induced HK-2 cells injury.

Background: Tubular injury is considered as a crucial pathological feature of diabetic nephropathy. LncRNA MALAT1 is involved in diabetic complications. Hence the role of MALAT1 in high glucose-induced renal tubular epithelial cells (HK-2) injury deserves investigation.

High glucose induces renal tubular epithelial injury via Sirt1/NF-kappaB/microR-29/Keap1 signal pathway.

Objective: Diabetic nephropathy (DN) is a serious complication that commonly confronted by diabetic patients. A common theory for the pathogenesis of this renal dysfunction in diabetes is cell injury, inflammation as well as oxidative stress. In this content, the detailed molecular mechanism underlying high glucose induced renal tubular epithelial injury was elaborated.

Long non-coding MIAT mediates high glucose-induced renal tubular epithelial injury.

Background And Objective: Long non-coding RNAs (lncRNAs) constitute a novel class of non-coding RNAs that take part in occurrence and development of diabetes complication via regulating gene expression. However, litter is known about lncRNAs in the setting of diabetes induced nephropathy. The aim of this study was to examine whether lncRNA-myocardial infarction-associated transcript (MIAT) is involved in diabetes induced renal tubules injury.

Down-regulation of miR-186 contributes to podocytes apoptosis in membranous nephropathy.

Background And Aim: Podocytes apoptosis is the key process in the development of membranous nephropathy and miR-186 is reported to be related with cell apoptosis. Here we investigated the expression of miR-186 in membranous nephropathy (MGN) patients and the mechanism underlying the podocytes apoptosis.

Methods: Thirty patients with MGN and 30 healthy people were included in this study.